The aim of this project was to further characterize the binding of aldosterone and other mineralocorticoids in human plasma and to support or deny the possibility suggested by others that aldosterone is bound in part to a specific binding protein. Further that this binding is altered in essential hypertension. Part of our objectives have been achieved. Using various types of molecular sieving chromatography (G-200) we find that aldosterone (3H) and cortisol (14C) binding of fresh human plasma includes just free albumin-bound, and CBG-like binding. To further characterize this binding we used electrophoresis and dialysis against albumin and authentic CBG. Again the binding of aldosterone could be explained entirely (20%) to CBG-transcortin. Finally in a series of displacement studies we have shown that all aldosterone binding can be displaced by cold aldosterone cortisol or progesterone. These studies further indicate that corticosteroid binding globulin accounts for all globulin binding of aldosterone. This work has been submitted for publication. New work this year will involve studies of aldosterone and DOC kinetics in hypertensive patients to determine if there is a defect in the peripheral metabolism of aldosterone to explain the significant increase in plasma aldosterone levels in low renin subjects apparently not due to increased secretion rates.